Kidney regeneration in Aphanius furcatus (Teleostei: Aphaniidae) after damage induced by gentamicin and evaluation of vitamin C in toxicity reduction

Gentamicin is known to stimulate the production of reactive oxygen species and lead to renal damage in some groups of vertebrates through oxidative stress. The kidney regeneration of the killifish Aphanius furcatus was studied after gentamicin-induced oxidative stress. In addition, we evaluated the possible role of vitamin C as an antioxidant in the reduction of renal toxicity. A total of 24 specimens (3.5-4cm in total length) were divided into four groups: In group-I two fish specimens treated with 7.5µl of normal saline injection; in group-II, 10 specimens received 10µg/g body weight (b.w) gentamicin; in group-III, two fish were treated with totally 60µg/g b.w vitamin C; and in group-IV, 10 specimens received both 10µg/g gentamicin and 60µg/g b.w vitamin C. The kidney tissues of group-I, III and IV were sampled during the nephrotoxicity phase (i.e., 10 hours post injection (hpi) to 5 days post injection (dpi)) and kidney tissues of group-II sampled daily for 10 dpi until regeneration completed. The kidney regeneration of A. furcatus through nephron neogenesis was detected by newly formed nephron on 8 dpi, and it is completed on 10 dpi. Our histological results in gentamicin-induced oxidative stress (group-II) clearly showed that the most severe damage is occurred in the kidney tissue within 1-4 dpi. However, in the specimens that antioxidant therapy supplied with vitamin C (group-IV), damage effect of gentamicin has remarkably repressed within these days. The outcome of this study revealed that administration of vitamin C is effective in reduction of gentamicin-induced nephrotoxicity in A. furcatus . Vitamin C reduces the toxicity effect of gentamicin by reduction of free radicals and reactive oxygen species (ROS) through its antioxidant activity. Therefore, using vitamin C together with gentamicin enhances the body resistance to the stress condition and reduces the toxicity effect of gentamicin.